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    Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2022 Jul 13. pii: S1542-3565(22)00642-5. doi: 10.1016/j.cgh.2022.06.007
    Carvedilol achieves higher hemodynamic response and lower rebleeding rates than propranolol in secondary prophylaxis.
    Jachs M1,  Hartl L2,  Simbrunner B3,  Bauer D4,  Paternostro R5,  Balcar L6,  Hofer B7,  Pfisterer N8,  Schwarz M9,  Scheiner B10,  Stättermayer AF11,  Pinter M12,  Trauner M13,  Mandorfer M14,  Reiberger T15
    Author information
    1Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    2Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    3Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Christian Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria.
    4Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    5Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    6Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    7Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Christian Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria.
    8Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Department of Internal Medicine IV, Klinik Landstraße, Vienna, Austria.
    9Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Department of Internal Medicine IV, Klinik Ottakring, Vienna, Austria.
    10Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    11Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    12Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    13Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    14Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
    15Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Christian Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria. Electronic address: thomas.reiberger@meduniwien.ac.at.
    Abstract

    BACKGROUND AND AIMS: Carvedilol induces stronger decreases in hepatic venous pressure gradient (HVPG) than conventional nonselective beta-blockers (NSBB), i.e., propranolol. Limited data exists on the efficacy of carvedilol in secondary prophylaxis of variceal bleeding.

    METHODS: Patients undergoing paired HVPG measurements for guiding secondary prophylaxis with either carvedilol or propranolol were included in this retrospective analysis. All patients also underwent band ligation. Changes in HVPG and systemic hemodynamics were compared between the two groups. Long-term follow-up data on rebleeding, acute kidney injury (AKI), non-bleeding decompensation and liver-related death was analyzed applying competing risk regression.

    RESULTS: Eighty-seven patients (carvedilol/propranolol: n=45/n=42) were included in our study. The median baseline HVPG was 21 (IQR: 18; 24) mmHg, and 39.1%/48.3%/12.6% had Child-Turcotte-Pugh-A/-B/-C cirrhosis, respectively. Upon NSBB initiation, HVPG decreased stronger in carvedilol users (relative decrease: -20 [-29; -10]% vs. -11 [-22; -5]% for propranolol, p=0.027), who also achieved chronic HVPG response more often (53.3% vs. 28.6%, p=0.034). Cumulative incidences for rebleeding (Gray's test: p=0.027) and liver-related death (p=0.036) were significantly lower in patients taking carvedilol, as compared to propranolol. Notably, ascites development/worsening was also less commonly observed in carvedilol patients (p=0.012). Meanwhile, AKI rates did not differ between the two groups (p=0.255). Stratifying patients by HVPG response status yielded similar results. The prognostic value of carvedilol intake was confirmed in competing risk regression models.

    CONCLUSIONS: Carvedilol induces more marked reductions in HVPG than propranolol in secondary prophylaxis of variceal bleeding, and is thus, associated with lower rates of rebleeding, liver-related death and non-bleeding further decompensation.


    Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.

    KEYWORDS: Cirrhosis, nonselective betablocker, portal pressure, variceal bleeding

    Publikations ID: 35842118
    Quelle: öffnen
     
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